Saturday, March 10, 2012

A Plague to Remember: The Untold Story of The Oak Trees

Photo from here
Photo from here

By Clinton French

        Oaks trees such as the black oak, the white oak, and the live oak are monuments in ecosystems. Many different organisms rely on them for home and food. In fact, Black and White oaks are what land markedly decide where Oak savannas can be in Western N. America and without them, Oak savannas in in Oregon and many other places could not exist. The Live Oak on the other hand is just majestic and beautiful in the way it grows. It grows in many places and is appreciated as an iconic tree. These trees were once pristine and untainted, but now a plague is upon them.
Photo from here
        The Plague I am referring to is called Sudden Oak Death(Phytophthora ramorum) or SOD for short. SOD is a water mold that popped up within the last 30 years. And this water mold reproduces by spore, or more specifically by two types of spores. It has two spore types for transmission and they are resting spores(chlamydospores) and swimming spores(zoospores), which do as they sound. The resting spores have the ability to last through harsh winters, while the swimming are motile and fragile and use water as a means to spread their disease with ease. This water mold with its spores at the ends of it is pictured to the right.
Photo from here
Photo from here














     SOD is a disease that kills and infects many species, but it effects no other species like it does Oaks. SOD has devastating effects on Oak trees. Once infected, a oak tree gets cankers, which are the bleeding looking things on the left, and the “bleeding” eventually discolors bark and kills said area, like in the picture to the right. This disease then has about a 50/50 chance of killing an oak tree flat out, as found in "Responses of oaks and tanoaks to the sudden oak death pathogen..." where it is said that mortality rates of various oaks range from 2.4% to 5.1%, while the infection rates range from 4.1% to 10.0%. From there, it makes the remaining population of oaks susceptible to other forms of death, such as beetle infestation. Thus, SOD has an effective kill rate of higher than just 50% since it opens trees up to infestations and such. If it were an infection between just oaks, then the problem wouldn’t that hard to solve, because the infected individuals could just be removed, but this is not the case.
Photo from here
        SOD has many other species of plants that it can infect, such as California bay laurels, Douglas firs, Rhododendrons, evergreen huckleberries, coast redwood, big leaf maples, and many others. Most of these species that get infected have a very low rate of mortality, but they do experience dieback (shown in the picture to the left). These species act as carriers or hosts to that disease and are used to spread the disease far and wide in their areas of growth. The rate at which they spread is so high that within a year SOD has spread as far 35km from the nearest known path of SOD in California(Meentemeyer, R et al, 2008). The California laurel has been the main reason for the spread of SOD in California, but it doesn’t exist in Oregon as abundantly as it does in California, so it thankfully wouldn’t have as much of an effect as it does in California when it spreads to Oregon.
        One of the other main things that has amplified the spread of this disease is that fact that SOD is an introduced pathogen. If it were native, then the pathogens effectiveness would be severely diminished, for the plants it effects would have had some time to evolve to have resistance to the disease. Oaks have had not time to obtain resistance, because 30 years is a short amount of time for an oak tree. SOD emerged in the last 30 years and it is theorized to have been a mix between two exotic pathogens that were probably from Asia. Also, this pathogen is not found in Asia, for the exotics from which it comes have not been tracked down, but they could feasible be tracked down given enough time and information.
        Another contributor to the problem is that conifers are more fit than Oaks. When a space is opened up in a forest, the space is usually filled with what is representative of what is around it. Thus, as Oaks decline, conifers replace them, for they are more prevalent. Thus making it so that oaks are able to be slowly pushed out as SOD creeps further in. This is tree in California now and will be in Oregon if SOD is allowed to spread into its borders further.
        There is no cure for SOD. With that being said, there is a treatment. This treatment is Phosphonate and it is injected into trees. The injection acts as a booster shot and makes it so that the trees thicken their cell walls so that the water molds spores cannot penetrate them, as is explained in "Protecting trees from Sudden Oak Death before Infection". It’s a pretty simple fix, after all, if the spores cannot get in, then they cannot kill. This Phosphonate can also be used to prolong the life of an already infected tree. Also, it has a long term cost that comes with it. The Phosphonate needs to be administered every 2 years, for that is the effective length of the dosage recommended.
        Currently, the only legislative counter measures have been to regulates nurseries. Theses regulations were put in place to slow the spread of SOD, because SOD was spreading rapidly to new populations due to nursery host plants being transported to new areas from California, which is how it probably got to curry county. There are groups such as suddenoakdeath.org which encourage people to become active in this rapidly growing problem.
        As I see it, SOD is a plague unto the populations of oaks everywhere it is present, and as it stands now, there is only one county in Oregon where the dreadful pathogen has been found, while it is rampant in 14 of California’s counties. In order to protect the Oaks in Oregon, something must be done, or else the marked decline oaks is upon us. So, it is my suggestion that a barrier of Phosphonated trees be created both at the border between California and Oregon and around curry county which is the only county in Oregon with SOD As shown in the diagram below. But the Phosphonate must be applied to more that just Oak trees for it to be a barrier, since other trees, such as Douglas firs and big leaf maples, can contract the disease as well. Also, Phosphonating an oak tree is essentially just applying a booster shot to it, so it should have the ability to be applied to other trees and have the same or very similar results. Now by applying the before mentioned barrier with all trees being Phosphonated, then an effective barrier is formed in which a line of immune trees. This barrier will keep the disease contained such that the disease will run its course in the contained area and the uninfected population will remain uninfected.
        This course of action or some course of action very similar will need to be taken or else the marked decline of oak trees is upon us, for SOD is the plague that could end oaks forever.





Citations:

Information:

http://www.suddenoakdeath.org/   

http://en.wikipedia.org/wiki/Sudden_oak_death
 
http://anrcatalog.ucdavis.edu/pdf/8426.pdf     

http://kellylab.berkeley.edu/storage/papers/2010-McPherson-etal-FEM.pdf 

Meentemeyer, R. , Anacker, B. , Mark, W. , & Rizzo, D. (2008). Early detection of emerging forest disease using dispersal estimation and ecological niche modeling. Ecological Applications, 18(2), 377-390.
 
Ellis, A. , Vaclavik, T. , & Meentemeyer, R. (2010). When is connectivity important? a case study of the spatial pattern of sudden oak death. Oikos, 119(3), 485-493.

Images:(In order of occurrence from left to right, then down)

Photo from http://www.haltonhelps.com/Tree%20hunt/photo%20contest%201%20white%20oak%20lavecchia.jpg

Photo from http://v2.cache1.c.bigcache.googleapis.com/static.panoramio.com/photos/original/37284941.jpg?redirect_counter=2

Photo from http://www.suddenoakdeath.org/wp-content/uploads/sod_imports/images/Pram.parke.jpg

Photo from http://upload.wikimedia.org/wikipedia/commons/1/1a/Sudden_Oak_Death.jpg

Photo from http://cisr.ucr.edu/images/sudden_oak_death_01.jpg

Photo from http://www.jgi.doe.gov/News/SODbay101.jpg

The last diagram was created by me, the author.

2 comments:

  1. Having lived in central Coastal California (Santa Cruz) near the very town where nursery stock evidently first introduced Phytophthora ramorum and having a strong fondness for the types of forest in northern California and southern Oregon where sudden oak death syndrome has killed so many trees, I feel a strong personal sense of loss and worry about the impact of this introduced pathogen. There are so many examples of introduced pathogens and invasive species wreaking havoc, it is sometimes hard to work up anger or worry about any one particular species or pathogen, given how many seem to be a threat. For me, sudden oak death syndrome and Port Orford root disease (also a Phytophthora) are the two pathogens that make me most concerned because of the particular trees and forest types that they attack for which I feel particular affection.

    Having said all that, every strategy for dealing with an invasive species has to carefully weigh the costs and benefits of that strategy and, in particular, the efficacy of a particular strategy. The injected phosphonate barrier around Curry County in southern Oregon proposed in this blog is definitively innovative and takes seriously the threat proposed by SOD, but the costs of such a barrier strike me as potentially staggering. How much does it cost to inject each tree? How many trees must be injected to produce an effective barrier? Even if such a barrier is constructed, would SOD still have a chance of spreading through the continued introduction of the pathogen through nursery stock? Would it need to be coupled with a stricter regimen of quarantines and tests for intra-U.S. nursery stock movement? Or would quarantines and tests of nursery stock prior to movement with the U.S. be a more cost effective approach? But would the impact on the nursery industry be acceptable? And how would the costs and benefits/efficacy of such an effort compare to those potentially engaged in to combat other invasive species and pathogens? We simply don't have the resources to combat every threat even if my personal vote would be for stopping SOD and Port Orford root disease. These seem to be the kinds of hard questions that must be answered.

    It is also possible that SOD has not spread farther into Oregon because the community structure of our forests and oak woodlands is sufficiently different from California that the disease does not have the potential to spread as rapidly here. This blog communicates quite effectively the distastrous effect of SOD in California and its lethality in oak trees. However, there are many details that aren't provided that are necessary for understanding this better (of course, it's impossible to provide all details in the limited format of a blog). It seems that California Laurel (Bay) is a key vector in the spread of the disease and north of the Siskiyou Mountains in southern Oregon, Laurel becomes relatively rare. The blog mentions Douglas-fir (which is quite common) as a potential carrier, but to what extent? I have not heard the same level of concern about SOD's effect on Douglas-fir or with regards to its potential as a carrier. The efficacy of potential carriers seems to be a critical detail. Perhaps the science hasn't figure this all out yet. Furthermore, if oak populations in Oregon are spaced farther apart relative to each other and relative to potential carriers, perhaps they are less vulnerable to being reached by the pathogen. All of these things need to be considered before making a full-out investment in a barrier or quarantine regimen.

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  2. One additional small point with regard to clarity in this blog. The author write that once a tree is infected, the "disease then has about a 50/50 chance of killing an oak tree flat out, as found in (McPerhson et al 2010) where it is said that mortality rates of various oaks range from 2.4% to 5.1%, while infection rates range from 4.1% to 10.0%." I found this a little confusing, the discrepancy between "a 50% chance of killing" and a "mortality rate of ... 5.1%", and after skimming the cited article, I realized that there are some key units missing in the reporting here. That is, while there is a 50% chance of a tree dying once infected, the mortality rates to which the blogger is referring are yearly rates of 2.4% /yr to 5.1% /yr as are the infection rates which should also be 4.1%/yr to 10.0%/yr within the population. Furthermore, if I read the article correctly (and I just skimmed it, I might be incorrect) the mortality rates are cumulative mortality rates for infected populations of oaks that include mortality not caused by the pathogen, mortality rates that would otherwise be .54%/yr to .75%/yr due to all causes other than the pathogen. This means that annual mortality rates increase by 4.4 - 6.8 times those of normal rates in a population once the pathogen is introduced, a fairly alarming figure itself. I guess the key point here is that it's important to include the units for the sake of clarity.

    In any case, I am glad that Clinton has highlighted this issue and written compellingly about it, because this pathogen is indeed a threat to trees and forests that we care about.

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